Ventricular septal defect

Ventricular septal defects (VSDs) represent the most common form of congenital heart disease, and can be located in any portion of the ventricular septum. It is a hole in the wall between the ventricles which allows blood to flow from the left to the right ventricle because of the high pressare gradient. The quantity of blood flowing through the defect depends on it size.

Superior Vena Cava
Pulmonary VeinsPulmonary ArteryPulmonary Veins
Left Atrium
Right Atrium
Left Ventricle
Right Ventricle
Inferior Vena Cava

-Fig. 4.2
Ventricular septal defect. The arrow indicates the shunt-.

Small ventricular septal defects do not involve overload for the heart and do not carry out problem for the child. Usually the only sign of their presence is a cardiac murmur and generally they heal over spontaneously during infancy. Large VSD involve a great pulmonary influx and an increase in pulmonary artery blood pressure (pulmonary hypertension). Children with this feature present signs of heart failure: dyspnea, feeding difficulties, poor growth, profuse perspiration, pallor. Heart failure requires medical treatment. The time for surgery (during the first year of life or before starting going to school) is determined on the basis of pulmonary pressure and VSD sizes. Cardiac catheterization gives the maximum amount of useful information in patients with VSD, specially in infants with evidence of a large left-to-right shunt or heart failure, and patients with evidence of increased pulmonary vascular resistance with moderate or small left-to-right shunts. The improvements in echocardiographic/Doppler techniques have yield to allow accurate diagnosis in many patients with isolated defects and delay or obviate the need for catheterization. Children with small VSDs are asymptomatic and have excellent long-term prognosis. Neither medical therapy nor surgery is indicated. Direct surgical repair is the preferred operative therapy in most centers. Indications for surgical repair in infancy are uncontrolled congestive heart failure, including growth failure or recurrent respiratory infection. Large defects, even in the absence of symptoms, are repaired prior to 2 years of age if associated with elevated pulmonary artery pressare. The VSD is closed by the application of a synthetic patch and it is successful in 98% of the cases. Nowadays for muscular VSD, sited in the lower part of the ventricular septum, which do not close spontaneously and present the indication for closure, a device for percutaneous closure is available, similar to the one for the ASD closure. For perimembraneous VSD, sited in the higher part of the septum near the aortic valve and the conduction system, surgery still represents the treatment of choice in the majority of cases, even if a device for transcatheter closure is available, because of a superior rate of complications.

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